Evidence map›Paper›PMID 22347449›Full record

ArticlePloS one2012

Ameliorated ConA-induced hepatitis in the absence of PKC-theta.

Xianfeng Fang, Ruiqing Wang, Jian Ma, Yan Ding, Weirong Shang, Zuoming Sun

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Mincle Signaling Promotes Con A Hepatitis.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Article
  13. Diacylglycerol Kinases in T Cell Tolerance and Effector Function.Frontiers in cell and developmental biology · 2016
    Review
  14. Article
  15. The Novel PKCθ from Benchtop to Clinic.Journal of immunology research · 2015
    Review
  16. Article
  17. Review
  18. Article
  19. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Xianfeng FangDivision of Immunology, Beckman Research Institute of the City of Hope, Duarte, California, United States of America.
Ruiqing Wang
Jian Ma
Yan Ding
Weirong Shang
Zuoming Sun
City of Hope · USBeckman Research InstituteEmory University · US

Funding

PKC-theta function in RORgammat-regulated Th17 differentiationR01AI053147 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SUN, ZUOMING · 2004 to 2015
$3.7M
Dissecting PKC-theta-regulated T cell functions in allograft rejectionR56AI072554 · NIAID · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI SUN, ZUOMING · 2010 to 2010
$415k
NIAID NIH HHS R01 AI053147NIAID NIH HHS R01-AI053147NIAID NIH HHS R56 AI072554NIAID NIH HHS R56-AI072554
6 · The paper itself

Abstract

Severe liver injury that occurs when immune cells mistakenly attack an individual's own liver cells leads to autoimmune hepatitis. In mice, acute hepatitis can be induced by concanavalin A (ConA) treatment, which causes rapid activation of CD1d-positive natural killer (NK) T cells. These activated NKT cells produce large amounts of cytokines, which induce strong inflammation that damages liver tissues. Here we show that PKC-θ(-/-) mice were resistant to ConA-induced hepatitis due to essential function of PKC-θ in NKT cell development and activation. A dosage of ConA (25 mg/kg) that was lethal to wild-type (WT) mice failed to induce death resulting from liver injury in PKC-θ(-/-) mice. Correspondingly, ConA-induced production of cytokines such as IFNγ, IL-6, and TNFα, which mediate the inflammation responsible for liver injury, were significantly lower in PKC-θ(-/-) mice. Peripheral NKT cells had developmental defects at early stages in the thymus in PKC-θ(-/-) mice, and as a result their frequency and number were greatly reduced. Furthermore, PKC-θ(-/-) bone marrow adoptively transferred to WT mice displayed similar defects in NKT cell development, suggesting an intrinsic requirement for PKC-θ in NKT cell development. In addition, upon stimulation with NKT cell-specific lipid ligand, peripheral PKC-θ(-/-) NKT cells produced lower levels of inflammatory cytokines than that of WT NKT cells, suggesting that activation of NKT cells also requires PKC-θ. Our results suggest PKC-θ is an essential molecule required for activation of NKT cell to induce hepatitis, and thus, is a potential drug target for prevention of autoimmune hepatitis.

Indexed as

AnimalsAutoimmune DiseasesConcanavalin AHepatitis, AnimalInflammationIsoenzymesLymphocyte ActivationMiceMice, KnockoutNatural Killer T-CellsProtein Kinase CProtein Kinase C-thetaConcanavalin AIsoenzymesPrkcq protein, mouseProtein Kinase CProtein Kinase C-theta

Identifiers

PMID22347449
PMCPMC3274545
OpenAlexW2007400388

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.